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122 Cards in this Set
- Front
- Back
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What are the 4 specific properties of Cardiac Cells?
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Automaticity
(Ability to initiate an impulse spontaneously and continuously) Contractility (Ability to respond mechanically to an impulse) conductivity (Ability to transmit an impulse along a membrane in an orderly manner) Excitability (Ability to be electrically stimulated) |
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How much time is represented in the smallest square of an ECG?
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0.04 seconds
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How much time is represented in the larger square of ECG?
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0.2 seconds
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What is the reaction of the heart to stimulation of the vagus nerve?
e.g. vasovagul - strain for BM |
Slows heart rate and drops blood pressure
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Autonomic Nervous system controls what actions of the heart?
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Rate / Speed / Strength
rate of impulse formation speed of conduction strength of contraction |
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P wave represents?
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Atrial depolarization, (top of heart activated)
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PR Interval represents?
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conduction time, How long the impulse takes from the SA Node to the AV node
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QRS Complex represents?
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Ventricular depolarization. The amt of time for impulses to travel thru all ventricles
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ST Segment represents?
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Very (EARLY) phase of ventricular repolarization.
*patients with MI and Angina will show change in this segment* |
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T Wave represents?
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Ventricular repolarization
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QT Interval represents?
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Entire ventricular cycle: depolarization and repolarization together.
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How many beats is a normal sinus rhythm?
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SA node fires at 60-100 bpm
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What is sinus bradycardia?
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Normal conduction, but too slow.
SA node fires < 60 bpm. It is a normal condition for aerobically trained athletes and during sleep. |
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What is a dysrhythmia associated with a well trained athlete?
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sinus bradycardia
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Treatment for sinus bradycardia include what? And what is the goal of tx?
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IV Atropine
Pacemaker may be required. Goal to increase HR |
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When would you intervene for a patient with sinus bradycardia?
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Only if/ when they are not tolerating the slow HR. The BP will go down, may become disoriented, dizzy, SOB.
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What is Sinus Tachycardia?
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Normal conduction, too fast. SA firing at >100 bpm. Result of vagal inhibition.
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What is the clinical significance of sinus tachycardia?
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Dizzy
Hypotension due to decrease CO Increase myocardial oxygen consumption could lead to angina The supply of oxygen can't meet the demand. |
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Tx for sinus tachycardia?
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Beta blocker ---reduce HR
Antipyretic -- reduce fever Analgesics -- tx pain |
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What is atrial flutter?
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Identified by recurring, regular, sawtooth-shaped flutter waves. It originates from a single ectopic focus.
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What is clinical significance of atrial flutter?
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-High ventricular rates >100
-loss of atrial "kick" decrease CO which can lead to HF, angina - risk for stroke to due to risk of clot form in the atria |
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Drugs to Tx atrial flutter?
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Antidysrhythmia drugs:
amiodarone, propafenone goal to slow ventricular response by increasing AV block |
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What if drugs dont work for atrial flutter? Is there another treatment?
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Radiofrequency catheter abalation:
"Mapping" -microwave energy to 'zap' the irritable spot... it goes dead and stops the rapid impulses |
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What is the most common abnormal rhythm? Whats the 2nd most common?
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Most common - Atrial Fibrillation
2nd - Atrial flutter |
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What is Atrial fibrillation?
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total disorganization of atrial electrial activity without effective atrial contraction
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What are the drugs used for tx of atrial fib?
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RATE CONTROL
Digoxin (slow) Beta Blockers (First drug of choice. Slows heart rate fastes) Ca Channel blockers Antidysrhythimic: used for conversion to reg sinus rhythm Amiodarone Propafenone AND long term anticoagulation: if been in A-Fib for > 48 hrs: Coumadin Goal of tx is to decrease ventricular response and to prevent embolic stroke. |
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Tx other than drugs for Atrial Fibrillation?
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Radiofrequency catheter ablation
Maze procedure |
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What is junctional dysrhythmia?
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dysrhythmia that originates in AV node. Slower, AV is the back - up so HR is 40-60.
No P wave |
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What drugs are used to tx junctional dysrhytmia?
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Atropine (if symptomatic)
beta blockers Ca channel blockers amiodarone for rate control digoxin is held DC cardioversion is contraindicated |
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What is 1st degree heart block?
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type of AV block in which every impulse is conducted to ventricles but the duration of AV conduction is PROLONGED
**just a delay at AV** **conduction still gets thru** • PR interval is longer than normal |
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TX for 1st degree heart block?
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No tx.
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What is 2nd degree heart block?
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Gradual lengthening of PR interval due to prolonged AV conduction time.
**atrial impulse nonconducted and a QRS is missing **predictable pattern, q 3rd beat doesn't come thru |
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What is junctional dysrhythmia?
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dysrhythmia that originates in AV node. Slower, AV is the back - up so HR is 40-60.
No P wave |
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What drugs are used to tx junctional dysrhytmia?
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Atropine (if symptomatic)
beta blockers Ca channel blockers amiodarone for rate control digoxin is held DC cardioversion is contraindicated |
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What is 1st degree heart block?
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type of AV block in which every impulse is conducted to ventricles but the duration of AV conduction is PROLONGED
**just a delay at AV** **conduction still gets thru** • PR interval is longer than normal |
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TX for 1st degree heart block?
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No tx.
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What is 2nd degree heart block?
Type I |
Gradual lengthening of PR interval due to prolonged AV conduction time.
**atrial impulse nonconducted and a QRS is missing **predictable pattern, q 3rd beat doesn't come thru **HR slows, how does pt tolerate? |
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TX for type 1 2nd degree heart block:
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digoxin
beta blockers if symptomatic, atropine or temporary pacemaker |
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What is 2nd degree heart block, type II?
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Nonconducted p wave, w/o prgressive antecent PR lengthening.
Usually block in bundle branches. **not stable ** its a sign that there is a more active heart disease *reduced HR results in decrease CO, leads to hypotension and MI |
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TX for 2nd degree heart block , type II?
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if symptomatic (hypotension, angina) permanent pacemaker
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What is 3rd degree heart block?
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Form of AV dissociation in which NO impulses from atria are conducted to ventricles.
almost always leads to decrease CO with subsequent ischemia, HF, and shock. syncope (loss of consciousness) may result from severe bradycaria or even asystole almost always very symptomatic |
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Tx of 3rd degree heart block?
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Drugs: atropine, epinephrine
permanent pacemaker ASAP... generally drugs don't work. |
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What is premature ventricular contractions?
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Contractions that originate in ectopic focus of the ventricles. premature occurance of a wide and distorted QRS complex
multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples, triplets, R on T phenomena |
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TX for PVC?
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2 questions:
1. what is the CAUSE? 2. HOW is patient doing? O2 therapy for hypoxemia electrolyte replacement Drugs: beta blockers, procainamide, amiodarone, (see a lot) lidocaine (old standard) |
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What is ventricular tachycardia?
(V-Tach) |
Run of 3 or more PVC's
LIFE THREATENING because of decrease CO and possibility of deterioration ventricular fib sustained / polymorphic / stable / unstable |
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V-tach usually two main causes:
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1. extreme cardiac problem (MI)
OR 2. extreme electrolyte problem |
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Tx for V-tach
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Identify & tx FAST!!
if stable (has pulse)... start with drugs. IV procainamide, sotalol, amiodarone, lidocaine unstable (pulseless) #1 start CPR #2 tx = defibrillation (shock with electrical current, shock irritable site back into functioning) **IV amiodarone or lidocaine followed by cardioversion** |
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What is Ventricular fibrillation?
V-Fib |
Severe derangement of the heart rhythm .
**irregular undulations of varying contour and amplitude on ECG **NO contraction **NO CO so many rapid firing irritable sites that ventricles are bombarded and just quiver |
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Tx for V-Fib?
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Immediate initiation of CPR - then defibrillation. if not treated rapidly, death results.
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What is the most common dysrhytmia associated with sudden death?
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Ventricular fibrillation
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What is asystole?
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flatline, no electrical activity.
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What are the 3 life-threatening dysrhytmias?
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V-tach
V-Fib Asystole |
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what are some causes of pulseless electrical activity?
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drug overdose
cardiac tamponade MI tension pneumothorax pulmonary emoblus |
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Tx for pulseless electrical activity?
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CPR followed by intubation and IV epinephrine
atropine if ventrical is slow |
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What is a common dysrhythmia that is treated wit hsynchronized cardioversion?
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A-fib
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A patient with an acute MI develops the following ECG pattern: atrial rate of 82 and regular. ventricaular rate of 46 and regular, p wave and QRS complex normal but there is no relationship between the p wave and QRS. the nurse identifies the arrhythmia as_____________ and tx indicated is ___________
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3rd degree heart block
pacemaker |
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A common arrhythmia the nurse would expect to find in a pt with hypoxemia and hypovolemia is _________
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sinus tachycardia
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An arrhythmia that is characterized by progressive lengthening of the PR interval until an atrial impulse is not conducted and a QRS complex is dropped is known as_______
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Type I, Second degree heart block
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PVC's that occur on the T wave of preceding contraction are always treated because they may precipitate _______ or _________
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V-tach or V-fib
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A patient with heart disease has a sinus bradycardia of 48 bpm. the nurse recognizes that the patient is at greatest risk for:
a. asystole b. heart block c. sinus arrest d. ectopic premature beats |
d. ectopic premature beats
Slow SA impulse may allow for escape arrhythmias to take over |
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A patient with an acute MI has a sinus tachycardia of 126 bpm. The nurse recognizes that if this arrhythmia is not treated, the pt is likely to experience
a. hypertension b. escape rhythms c. ventricular tachycardia d.an increase in infarct size |
d.an increase in infarct size
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A pt with no history of heart disease has a rhythm strip that shows an occasional distorted P wave followed by normal AV and ventricular conduction. The nurse questions the patient about:
a. use of caffeine b. use of sedatives c. aerobic training d. holding breath during exertion |
a. use of caffeine
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A patient's rhythm strip indicats a normal heart rate and rhythm with normal Pwave and QRS complex, but the PR interval is long . Them ost appropriate action by nurse is to
a. continue to assess pt b. admin atropine c. prepare for synchronized cardioversion |
a. continue to assess pt
Its first degree heart block |
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In the patient with an arrhythmia, the nurse identifies a nrusing dx of decreased cardiac output related to arrhyhtjmias when the pt experiences
a. hypertension and bradycardia b. chest pain and decreased mentation c. abdominal distention and patmegally d. bounding pulse and ventricular heave |
b. chest pain and decreased mentation
symptoms of decreased CO related to cardiac arrhythmias include a sudden drop in BP and symptoms of hypoxemia, such as decreased mentation, chest pain, and dyspnea. Peripheral pulses are weak and heart rate may be increased or decreased depending on the dysrhythmia |
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Patient with acute MI is having multifocal PVCs and ventricular couplets. He is alert and has a bp of 118/78 with an irreg pulse of 86 bpm. the most appropriate action by the nurse at this time is to
a. continue to assess the pt b. be prepared to admin CPR c. admin antiarrhythmic drugs per protocol d. ask the pt to perform valsava |
c. admin antiarrhythmic drugs per protocol
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Premature ventricular contractions are indicated by a rhythm pattern finding of
a. a wide QRS complex followed by a p wave b. continuous wide QRS complexes with vent. rate of 160 bpm c. sawtooth p waves d. p waves hidden in QRS complex with reg rhythm |
a. a wide QRS complex followed by a p wave
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Following fibrinolytic therapy, the nurse monitors the pt for the common reperfusion arrhythmias of
a. sinus tachycardia and atrial fib b. premature atrial and ventricular contractions c. premature ventricular contractions and ventricular tachycardia |
c. premature ventricular contractions and ventricular tachycardia
The most common arrhythmias to occur when the myocardium is reperfused following thrombolytic therapy are PVCs and ventricular tachycardia, and their presence may be an indicator of the success of the therapy |
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A patient in the coronary care unit develops V-fib. within protocol guidelines, the first action the nurse should take is to
a. initiate CPR b. perform defib c. prepare for cardioversion d. admin antiarrhythmic drugs |
b. perform defib
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Cardiac defib
a. enhances repolarization and relaxation of ventricular myocardial cells b. provides an electrical impulse that stimulates normal myocardial contractions c. depolarizes the cells of myocardium to allow the SA node to resume pacemaker function d. delivers an electrical impulse to the heart at the time of vent contraction to convert the heart to a sinus rhythm |
. depolarizes the cells of myocardium to allow the SA node to resume pacemaker function
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Initial tx of asystole and pulseless electrical activity is
a. CPR b. Defib c. admin atropine d. admin epinephrine |
a. CPR
during asystole or pulseless electrical acitvity, CPR must be initiated immediately to maintain minimal cardiac output and oxygentation followed by intubation and admin of epinephrine and atropine. defib is not effective because the myocardial cells are in state of depolarization |
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Nurses responsibilites in preparing to admin defib include
a. applying gel pads to pt's chest b. setting defib level c. setting synch mode d. sedating patient |
a. applying gel pads to pt's chest
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The use of catheter ablation therapy to "burn" areas of the cardiac conduciton system is indicated for tx of
a. sinus arrest b. heart bblocks c. tachyarrhythmias d. multifocal ectopic foci |
c. tachyarrhythmias
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What is the standard lab test for MI?
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Troponin
Level rises after an event occurs, (4-6 hrs) & peaks sooner, stays elevated LONGER. Is released in response to hypoxia |
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Elevated or depression of ST segment during chest pain can indicate what?
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MI
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When myocardial ischemia is temporary and reversible, the condition is called:
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stable angina
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the three conditions that are included as manifestations of acute coronary syndrome are:
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unstable angine
non-STEMI STEMI |
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When myocardial cells die as a result of ischemia, the area of cellular necrosis is known as:
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infarction
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Myocardial ischemia occurs as a result of two factors:
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increased O2 demand
decreased O2 supply |
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What is affected and what changes are on the ECG of a Non-ST elevation MI (NSTEMI)
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(non Q-wave MI or subendocardial MI)
Affects endocardium & myocardium ECG changes are: ST - depression T wave inversion (also see those ECG changes with unstable angina) |
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What is affected and what changes or on the ECG of an ST elevation MI (STEMI)
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(Q-wave or transmural MI)
Affects all three layers of myocardium ECG: ST elevation HAS Q waves |
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What are the developmental stages of atherosclorosis:
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1. Fatty streak
(charactereized by lipid-filled smooth muscle cells) 2. Raised fibrous plaque (beginning of progressive stages in artery walls, chronic endothelial injury) 3. Complicated lesions (most dangerous. Plaque consists of a core of lipid material - within an area of dead tissue) |
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Unstable Angina or NonSTEMI ECG pattern:
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• depression of ST segment
• inverted T-wave Means that pt HAS a bloodflow, but it is not enough to meet the demands of the heart. Having an MI. |
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STEMI ECG pattern:
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• ST-elevation
"tombstone pattern" Means that a clot is totally blocking the bloodflow to the heart. |
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Risk stratification for MI
HIGH risk: History / Exam / ECG / Cardiac markers |
• History:
-Pain like prior angina -know hx of CAD or past MI • Exam -Transient MR (?) - Hypotension - Diaphoresis - Pulmonary edema - Crackles • ECG - Transient ST-segment changes > 0.05 or T-wave inversion > 0.2 with symptoms • Cardiac markers: -Elevated troponin. This pt is having an MI RIGHT NOW!! |
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Risk stratification for MI
INTERMEDIATE risk: History / Exam / ECG / Cardiac markers |
• History
- Chest/ left arm pain - Age > 70 - Male - Diabetic • Exam - Extracardiac vascular disease • ECG - Fixed Q-waves -Abnormal ST-segments or T-waves • Cardiac markers: -normal This is non-definitive... |
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Risk stratification for MI
LOW risk: History / Exam / ECG / Cardiac markers |
• History
- Probable ischemic symptoms; no high or intermediat signs - OR recent cocaine use • Exam -Chest discomfort reproduced by palpatation (could be bruising and not cardiac at all) • ECG - T-wave flattening - OR normal • Cardiac markers -normal |
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Acute interventions for MI risk include:
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• Oxygen (if having pain, its from hypoxia)
• Aspirin ( reduces platelet aggregation. do immediately! do NOT us COATED. Have pt chew up pill, get in system ASAP) • Heparin (prevent further throbus formation. usually follow and IV protocol according to PTT) • Plavix / Ticlid (receptor antagonists. start immediately) • Glycoprotein IIb/IIIa inhibitors (assists with cath-labs) • Nitroglycerin (vasodialator. chest pain relief, monitor BP. give sublingual, IV, or capsul. RE-establis the Blood flow! * IV may stop being effective, switch to sublingual * most worried about ypotension * pt will get headaches • Morphine (decrease anxiety! vasodialator. give in small frequent boluses. * monitor BP * Monitor Resp rate (if pt is actively having pain... they WILL breathe.) |
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Name 2 types of reperfusion strategies after / during MI:
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• Primary PCI
(Primary PCI is treatment that occurs while the blood clot is still forming - usually within 12 hours of onset - - greater than 3 hrs of symptom onset -- and under 90 min of first med contact, but ideally within 2 hours of onset of symptoms.) • Fibrinolysis (is the process wherein a fibrin clot, the product of coagulation, is broken down. Tx if less than 3 hrs from onset of smptoms and /or unable to perform invasive strategies). |
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What are two of the biggest complications after an MI?
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Dysrhythmia...
V-tach / V-fib / Asystole are life threatening. Heart failure - pumping power diminished |
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What is the goal on scale 0-10 for chest pain?
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"0"
Any pain indicates ischemia / hypoxia Priority tx = PAIN FREE |
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What is the syndrome that can result from any structural or functional cardiac disorder that IMPAIRS the ability of the ventricle to FILL or EJECT blood?
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Heart Failure
Its the inability of heart to pump enough blood to meet the demands of the body |
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These signs indicate what kind of heart failure?
• systemic venous congestion, JVD, peripheral edema, heptaomegaly, elevated CVP (central venous pressure) |
RIGHT sided heart failure
ineffective Right Ventricle contractility. Can be caused from Left heart failure, pulmonary edema, pulmonary HTN, COPD, & RVMI (right vent. myocardial infarction) |
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These signs indicate what kind of heart failure?
• Decreased CO and systemic perfusion, pulmonary congestion |
LEFT heart failure
ineffective LV contractillity due to: MI, HTN, valvular disease |
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These signs indicate what kind of heart failure?
• inability of ventricles to eject adequate volume • decreased CO • increased SVR • EF < 40% |
SYSTOLIC heart failure
Due to: MI, dilated cardiomyopathy, congenital heart disease, valvular disease, HTN, alcohol |
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These signs indicate what kind of heart failure?
• inability of ventricles to RELAX & FILL • increased filling pressure • more frequent in elderly & women w/ HTN |
DIASTOLIC heart failure
Due to: HTN, restrictive or hypertrophic cardiomyopathy, valvular disease |
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What is the syndrome that can result from any structural or functional cardiac disorder that IMPAIRS the ability of the ventricle to FILL or EJECT blood?
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Heart Failure
Its the inability of heart to pump enough blood to meet the demands of the body |
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These signs indicate what kind of heart failure?
• systemic venous congestion, JVD, peripheral edema, heptaomegaly, elevated CVP (central venous pressure) |
RIGHT sided heart failure
ineffective Right Ventricle contractility. Can be caused from Left heart failure, pulmonary edema, pulmonary HTN, COPD, & RVMI (right vent. myocardial infarction) |
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These signs indicate what kind of heart failure?
• Decreased CO and systemic perfusion, pulmonary congestion |
LEFT heart failure
ineffective LV contractillity due to: MI, HTN, valvular disease |
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These signs indicate what kind of heart failure?
• inability of ventricles to eject adequate volume • decreased CO • increased SVR • EF < 40% |
SYSTOLIC heart failure
Due to: MI, dilated cardiomyopathy, congenital heart disease, valvular disease, HTN, alcohol |
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These signs indicate what kind of heart failure?
• inability of ventricles to RELAX & FILL • increased filling pressure • more frequent in elderly & women w/ HTN |
DIASTOLIC heart failure
Due to: HTN, restrictive or hypertrophic cardiomyopathy, valvular disease |
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These signs indicate what kind of heart failure?
• Inadequate delivery of blood and hypoperfusion of organs • decreased CO • Increased SVR |
FORWARD heart failure
Due to: aortic stenosis, HTN |
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These signs indicate what kind of heart failure?
• Failure of the ventricles to EMPTY completely • EF <40% • Pulmonary congestion |
BACKWARD heart failure
Due to: LV systoic congestion |
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These signs indicate what kind of heart failure?
• Sudden onset, heart overwhelmed and compensatory mechanisms have not been activated • Acute pulmonary edema, cardiogenic shock |
ACUTE heart failure
brand new condition. OR chronic condition is overwhelmed and body can no longer compensate |
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These signs indicate what kind of heart failure?
• Ongoing, compensatory mech are active and have had the ability to partially or completely restore cardiac function • Catcholamine levels elevated • Structural heart chamber changes |
CHRONIC heart failure
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At which stage of heart failure is there structural damage AND physical symptoms?
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Stage C
A= not in heart failure, have risk factors B= Structural damage, no symptoms C= Structural damage & symptoms D= Structural & physical symptoms to the point that intervention is needed to be functional |
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If a patient presents with SOB and crackles in lung, what test is done to determine if this is pneumonia or heart failure?
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Test levels of BNP or NT-proBNP
BNP = elevated levels suggest amt of heart failure, the higher the # the more stretching the heart muscle is doing and the more severe NT-proBNT= Quickly determines YES/NO to heart failure. Its fast and helpful in the ER |
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What is the best treatment for heart failure?
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PREVENTION
Tx is focused on stages, stop at earliest stage |
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The heart has an inability to pump blood, and has decrease in ejection fraction, this disorder is:
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Systolic heart failure
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Heart has impaired ability of the ventricle to fill during diastole, which results in decreased stroke volume, this disorder is:
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Diastolic heart failure
Also, the dx of this is made on the basis of the presence of pulmonary congestion and pulmonary htn with a NORMAL ejection fraction |
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Which type of cardiomyopathy should NOT be treated with inotropes?
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Hypertrophic
don't want to strengthen the contraction, want to slow down contraction/ squeeze gentler Tx with beta blockers, Ca blockers, antidysrhythmics, anticoag. The other two cardiomyopathies can be treated with inotropes |
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Is cardiomyopathy reversible?
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No. Its permanent damage.
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Which cardiomyopathy is termed the "muscle bound heart"
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Hypertrophic cardiomyopathy
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Which cardiomyopathy has systolic dysfunction?
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Dilated Cardiomyopathy.
Hypertrophic and restrictive have diastolic dysfunction. |
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What is going on if a patient has a weak floppy heart? And lots of congestion?
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Dialated Cardiomyopathy
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In regards to HTN, what lifestyle modification would have the best outcome for preventing HTN?
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Weight reduction.
LEss tissue to perfuse! |
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What is the difference between HTN emergency vs. HTN urgency?
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Emergency has evidence of end-organ damage
Urgency is elevated bp without organ damage. |
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Thrombi from right side of the heart is most likely due to:?
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long term A-fib or A-flutter
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Classic triad of symptoms of a pulmonary emoboli are?
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Dyspnea
Chest pain Hemoptysis |
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What disease is present if a patient has sharp stabbing chest pain, and friction rub sound on auscultation?
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Pericarditis
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Pericarditis is best treated with?
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NSAIDS
tx cause of inflammation |
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Upon auscultation the heart is sounding muffled. This could be a sign of?
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Cardiac tamponade
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Name some reasons a patient would need a coronary artery bypass instead of an angioplasty?
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• Failed medical tx
• Blockage at left coronary artery • Not a candidate for PCI • Failed PCI with ongoing chest pain |
